TPOAb

This study investigates the role of fatty acid oxidation in the pathogenesis of Hashimoto's thyroiditis (HT) and its impact on CD4+ T cell differentiation. The imbalance between Treg and Th17 cells is a hallmark of HT, with Th17 cells being abnormally activated. The results show that fatty acid oxidation, particularly through the mTOR/ACC1/CPT1A pathway, plays a significant role in this process. In both in vitro and in vivo experiments, increased expression of key fatty acid oxidation proteins was observed in CD4+ T cells from HT patients and in EAT mice models. Treatment with Etomoxir, an inhibitor of fatty acid oxidation, reversed the abnormal differentiation of CD4+ T cells and ameliorated the severity of HT by reducing inflammation and lymphocyte infiltration in the thyroid. These findings suggest that targeting the fatty acid oxidation pathway could offer a potential therapeutic strategy for modulating immune responses and treating autoimmune thyroid diseases such as Hashimoto's thyroiditis.